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F. A. CAJORI, Ph.D.; C. Y. CROUTER, M.S.; RALPH PEMBERTON, M.D.

Arch Intern Med. 1924;34(4):566-572.

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In 1858 Richardson¹ published the results of extensive experiments on dogs in which the injection of large quantities of lactic acid, intraperitoneally, was followed by severe joint involvement. The condition of the joints was similar to that seen in acute arthritis, and Richardson suggested that the arthritic syndrome was due to an accumulation of lactic acid in the body. This theory found further support in 1877, when Foster² reported that the administration of lactic acid by mouth to two diabetic patients resulted in painful and swollen joints. The pain and swelling persisted as long as the lactic acid administration was continued and disappeared promptly after the acid was discontinued. These early experiments were apparently never repeated or extended but they have exerted some influence in the formation of hypotheses regarding the disease. Within very recent years, for example, the theory that arthritis and muscular rheumatism are characterized by an excessive . . . [Full Text PDF of this Article]

Author Affiliations
PHILADELPHIA

Footnotes
From the Laboratory of Clinical Chemistry, Presbyterian Hospital. The work here reported is part of a study on chronic arthritis in collaboration with Robert B. Osgood, M.D., of Boston. The expenses of the investigation were defrayed by contributions from several sources, including a number of patients.

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